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27Background: Stark racial disparities in disease incidence among American women remains a persistent 28 public health challenge. These disparities likely result from complex interactions between genetic, social, 29 lifestyle, and environmental risk factors. The influence of environmental risk factors, such as chemical 30 exposure, however, may be substantial and is poorly understood. 31Objectives: We quantitatively evaluated chemical-exposure disparities by race/ethnicity and age in United 32 States (US) women by using biomarker data for 143 chemicals from the National Health and Nutrition 33 Examination Survey (NHANES) 1999(NHANES) -2014 Methods: We applied a series of survey-weighted, generalized linear models using data from the entire 35 NHANES women population and age-group stratified subpopulations. The outcome was chemical 36 biomarker concentration and the main predictor was race/ethnicity with adjustment for age, socioeconomic 37 status, smoking habits, and NHANES cycle. 38Results: The highest disparities across non-Hispanic Black, Mexican American, Other Hispanic, and other 39 race/multiracial women were observed for pesticides and their metabolites, including 2,5-dichlorophenol, 40 o,p'-DDE, beta-hexachlorocyclohexane, and 2,4-dichlorophenol, along with personal care and consumer 41 product compounds. The latter included parabens, monoethyl phthalate, and several metals, such as mercury 42 and arsenic. Moreover, for Mexican American, Other Hispanic, and non-Hispanic black women, there were 43 several exposure disparities that persisted across age groups, such as higher 2,4-and 2,5-dichlorophenol 44 concentrations. Exposure differences for methyl and propyl parabens, however, were the starkest between 45 non-Hispanic black and non-Hispanic white children with average differences exceeding 4 folds. 46 Discussions: We systematically evaluated differences in chemical exposures across women of various 47 race/ethnic groups and across age groups. Our findings could help inform chemical prioritization in 48 designing epidemiological and toxicological studies. In addition, they could help guide public health 49 interventions to reduce environmental and health disparities across populations.50 51 52The stark racial disparities in disease incidence and health outcomes among American women 53 remains a persistent public health challenge. For example, preterm birth incidence was found to be 54 approximately 60% higher in non-Hispanic Black women relative to non-Hispanic white women (Culhane 55 and Goldenberg 2011). Non-Hispanic Black and Hispanic women are at increased risk of being diagnosed 56 with developing dysglycemia (Marcinkevage et al. 2013) and diabetes (Cowie et al. 2009), relative to non-57 Hispanic white women. Non-Hispanic Black women are also 2-3 times more likely to develop the most 58 aggressive subtype of breast cancer, triple negative, compared to non-Hispanic white women (Carey et al. 59 2006; Stark et al. 2010). Furthermore, relative to non-Hispanic white women, non-Hispanic Black women...

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The rapidly growing field of toxicoepigenetics seeks to understand how toxicant exposures interact with the epigenome to influence disease risk. Toxicoepigenetics is a promising field of environmental health research, as integrating epigenetics into the field of toxicology will enable a more thorough evaluation of toxicant-induced disease mechanisms as well as the elucidation of the role of the epigenome as a biomarker of exposure and disease and possible mediator of exposure effects. Likewise, toxicoepigenetics will enhance our knowledge of how environmental exposures, lifestyle factors, and diet interact to influence health. Ultimately, an understanding of how the environment impacts the epigenome to cause disease may inform risk assessment, permit noninvasive biomonitoring, and provide potential opportunities for therapeutic intervention. However, the translation of research from this exciting field into benefits for human and animal health presents several challenges and opportunities. Here, we describe four significant areas in which we see opportunity to transform the field and improve human health by reducing the disease burden caused by environmental exposures. These include (1) research into the mechanistic role for epigenetic change in environment-induced disease, (2) understanding key factors influencing vulnerability to the adverse effects of environmental exposures, (3) identifying appropriate biomarkers of environmental exposures and their associated diseases, and (4) determining whether the adverse effects of environment on the epigenome and human health are reversible through pharmacologic, dietary, or behavioral interventions. We then highlight several initiatives currently underway to address these challenges.

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